ArticleAmerican journal of translational research2025
Leonurine alleviates doxorubicin-induced myocarditis in mice via MAPK/ERK pathway inhibition.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- A mugwort-based Chinese herbal mixture of five herbs improved oviduct health in laying hens under LPS challenge.Poultry science · 2026Article
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5 authors.
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Abstract
objectiveTo investigate the effects of naturally derived leonurine (Leo) on doxorubicin (Dox)-induced myocarditis and analyze its potential mechanisms.
methodsDox was intraperitoneally injected to establish a myocardial injury model in mice. The effect of Leo on inflammatory cytokine levels in myocardial tissue was assessed by ELISA. Pathological changes in myocardial tissue and apoptosis in myocardial cells were observed using hematoxylin-eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Protein levels were analyzed by Western blot (WB). Mouse myocardial H9c2 cells were divided into control group, Dox group, Leo (10 μmol/L) + Dox group, and Leo (20 μmol/L) + Dox group. Cell viability was assessed using Cell Counting Kit-8 (CCK8), and the levels of inflammatory cytokines were measured. The oxidation level and protein levels in H9c2 cells were also detected.
resultsLeo significantly reduced the levels of inflammatory cytokines in both serum and cell culture supernatant. Additionally, Leo also decreased the levels of inflammatory cytokines in cardiac tissue. Moreover, Leo suppressed Dox-induced myocardial cell apoptosis by modulating the BCL2 signaling pathway. In vitro studies revealed that both inflammatory cytokines and oxidative stress markers were decreased after treatment with Leo.
conclusionLeo exerts significant cardioprotective effects through anti-inflammatory mechanisms, likely mitigating Dox-induced myocardial inflammation by inhibiting the activation of MAPK/ERK pathways. These findings highlight Leo's potential as a promising cardioprotective agent, underscoring its therapeutic promise.
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